Abstract

Objective: The non-alcoholic fatty liver disease (NAFLD) is associated with cardiovascular events. At the same time a subclinical carotid change is associated with mortality and morbidity in hypertension. However it's unclear if there is a relationship between NAFLD and subclinical carotid damage in essential hypertension (EH). We searched for relationships between biochemical non-invasive NAFLD scores and subclinical carotid damage in a group of naïve EH patients. Design and method: In 299 naïve EH subjects (age 50 ± 13 years, 132 males) we evaluated clinical characteristics, biochemical scores of liver steatosis, as liver Fat Score (LFS), and fibrosis, as NAFLD Fibrosis Score (NFS), APRI, Fibrometer, and FIB-4, presence of echographic steatosis, metabolic syndrome, diabetes, levels of glucose, insulin, HOMA, lipids, glomerular filtration rate (GFR), reactive C protein (RCP), liver tests, platelet count, smoking habit and physical activity. By ultrasound carotid examination we measured the intima-media thickness (IMT), presence of carotid plaques, and in 115 subjects we calculated the carotid stiffness indexes, as the distension coefficient, the beta-stiffness, and the Young elastic module. Results: The IMT significantly increased across quartiles of LFS (P = 0.036), NFS (P = 0.001) and FIB-4 (P = 0.003). IMT was independently associated with FIB-4 (B = 0.380, P = 0.003) and NFS (B = 0.221, P = 0.013) scores. A IMT > 0.9 mm was independently associated with FIB-4 (P = 0.042). Patients with plaques had higher APRI (P = 0.005), Fibrometer (0.023), NFS (P < 0.001) and FIB-4 (P = 0.005) scores, and prevalence of plaques increased progressively across quartiles of LFS (P = 0.046), NFS (P < 0.001) and FIB-4 (P = 0.005). There was an independent association between carotid distension coefficient and Fibrometer (B = -0.360, P = 0.029), and between beta-stiffness and Fibrometer (B = 0.340, P = 0.036). Conclusions: In naïve EH patients the carotid IMT and carotid stiffness are independently associated with non-invasive NAFLD indexes. This association could induce to a more careful evaluation of a non-alcoholic liver damage in EH patients with subclinical carotid alterations. Moreover, studies are needed to clarify if profibrotic mechanisms are the base of both damages.

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